From Archives of Disease in Childhood, 25 April 2013 [Epub ahead of print].
Depression in paediatric chronic fatigue syndrome.
Bould H, Collin SM, Lewis G, Rimes K, Crawley E.
School of Social and Community Medicine, University of Bristol, , Bristol, UK.
Abstract
OBJECTIVE:
To describe the prevalence of depression in children with chronic fatigue syndrome (CFS)/myalgic encephalomyelitis (ME) and investigate the relationship between depression in CFS/ME and clinical symptoms such as fatigue, disability, pain and school attendance.
DESIGN:
Cross-sectional survey data using the Hospital Anxiety and Depression Scale (HADS) collected at assessment.
SETTING:
Specialist paediatric CFS/ME service in the South West.
PATIENTS:
Children aged 12-18 years with CFS/ME.
MAIN OUTCOME MEASURE:
Depression was defined as scoring >9 on the HADS depression scale.
RESULTS:
542 subjects had complete data for the HADS and 29% (156/542) (95% CI 25% to 33%) had depression.
In a univariable analysis, female sex, poorer school attendance, and higher levels of fatigue, disability, pain, and anxiety were associated with higher odds of depression.
Age of child and duration of illness were not associated with depression. In a multivariable analysis, the factors most strongly associated with depression were disability, with higher scores on the physical function subscale of the 36 item Short Form (SF-36).
CONCLUSIONS:
Depression is commonly comorbid with CFS/ME, much more common than in the general population, and is associated with markers of disease severity. It is important to screen for, identify and treat depression in this population.
From ‘Frontiers in Physiology', 19 April 2013.
Neurocognitive impairment in childhood chronic fatigue syndrome.
Kei Mizuno (1,2,3) and Yasuyoshi Watanabe(1).
1. Pathophysiological and Health Science Team, RIKEN Center for Life Science Technologies Kobe City, Hyogo, Japan
2. Department of Physiology, Osaka City University Graduate School of Medicine Osaka, Japan
3. Department of Medical Science on Fatigue, Osaka City University Graduate School of Medicine Osaka, Japan.
Abstract
Neurocognitive impairment is a feature of childhood chronic fatigue syndrome (CCFS). Several studies have demonstrated reduced attention control in CCFS patients in switching and divided attention tasks.
In students, the extent of deterioration in task performance depends on the level of fatigue. Poor performance in switching and divided attention is common in both fatigued students and CCFS patients. Additionally, attentional functions show dramatic development from childhood to adolescence, suggesting that abnormal development of switching and divided attention may be induced by chronic fatigue.
The brain structures associated with attentional control are situated inthe frontal and parietal cortices, which are the last to mature, suggesting that severe fatigue in CCFS patients and students may inhibit normal structural and functional development in these regions.
A combination of treatment with cognitive behavioral therapy and antidepressant medication is effective to improve attentional control processing in CCFS patients. Studies identifying the features of neurocognitive impairment in CCFS have improved our current understanding of the neurophysiological mechanisms of CCFS.
From Frontiers in Physiology, 1 May 2013.
Neuromuscular strain as a contributor to cognitive and other symptoms in Chronic Fatigue Syndrome: Hypothesis and conceptual model.
Peter C. Rowe (1), Kevin R Fontaine (2) and Richard L Violand (3).
1. Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 2. Department of Health Behavior, University of Alabama School of Public Health, Birmingham, AL, USA
3. Violand and McNerney, PA, Ellicott City, MD, USA
Abstract
Individuals with chronic fatigue syndrome (CFS) have heightened sensitivity and increased symptoms following various physiologic challenges, such as orthostatic stress, physical exercise, and cognitive challenges. Similar heightened sensitivity to the same stressors in fibromyalgia (FM) has led investigators to propose that these findings reflect a state of central sensitivity.
A large body of evidence supports the concept of central sensitivity in FM. A more modest literature provides partial support for this model in CFS, particularly with regard to pain. Nonetheless, fatigue and cognitive dysfunction have not been explained by the central sensitivity data thus far. Peripheral factors have attracted attention recently as contributors to central sensitivity.
Work by Brieg, Sunderland, and others has emphasized the ability of the nervous system to undergo accommodative changes in length in response to the range of limb and trunk movements carried out during daily activity. If that ability to elongate is impaired—due to movement restrictions in tissues adjacent to nerves, or due to swelling or adhesions within the nerve itself — the result is an increase in mechanical tension within the nerve.
This adverse neural tension, also termed neurodynamic dysfunction, is thought to contribute to pain and other symptoms through a variety of mechanisms. These include mechanical sensitization and altered nociceptive signaling, altered proprioception, adverse patterns of muscle recruitment and force of muscle contraction, reduced intra-neural blood flow, and release of inflammatory neuropeptides.
Because it is not possible to differentiate completely between adverse neural tension and strain in muscles, fascia, and other soft tissues, we use the more general term “neuromuscular strain.”
In our clinical work, we have found that neuromuscular restrictions are common in CFS, and that many symptoms of CFS can be reproduced by selectively adding neuromuscular strain during the examination. In this paper we submit that neuromuscular strain is a previously unappreciated peripheral source of sensitizing input to the nervous system, and that it contributes to the pathogenesis of CFS symptoms, including cognitive dysfunction.
The outcome of the last (physiological) study into neuromuscular strain looks more interesting than I had initially anticipated especially the concept of reduced intraneural blood flow. Further evidence, as if any more was needed, that exercise exacerbates pain, inflammatory and neurological symptoms in ME/cfs.